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Module 202 Theme 2 > Physiology of pain 2 > Flashcards

Physiology of pain 2 Flashcards

1
Q

What is meant by chronic pain?

A

greater than 3 months

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2
Q

What is meant by acute pain?

A

Less than 3 months

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3
Q

Give examples of acute pain

A

Following surgery
Musculoskeletal injury
Burn

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4
Q

Describe inflammatory pain

A

Due to tissue injury or inflammation

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5
Q

What is peripheral sensitisation?

A

Leads to pain hypersensitivity (hyperalgesia)
Reduction in the threshold of TRPV1 channels (by bradykinin, nerve growth factor)
Reduction in threshold in Na+ channels (prostaglandins)

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6
Q

What are the sites of treatment for acute pain?

A

PNS (site of injury)
CNS
Both

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7
Q

Describe local anaesthetics and how they work

A

Lidocaine or lignocaine
Topically applied to the skin
Sodium channel blockers - prevent nociceptor firing

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8
Q

Describe capsaicin treatment

A

Component of chilli peppers
TRPV1 channel agonist
Repeated uses reduce nociceptor firing
Mechanism of action - depletes substance P causes peripheral terminals to die back

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9
Q

Describe nonsteroidal antiinflammatory drugs and their mechanism of action

A

Eg. aspirin and ibuprofen
Reduces the inflammatory response by inhibiting prostaglandin synthesis - prevents peripheral sensitisation

Cyclooxygenase inhibitor - prostaglandin synthesis reduced - prevents decrease in Na+ channel threshold

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10
Q

Describe the action of paracetamol/acetaminophen

A

Not NSAID
Mechanism of action:- Inhibits cyclooxygenase (COX) enzymes (But does not reduce inflammation)
- Acts on descending serotonergic pathways

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11
Q

Describe the action of opiods

A

Eg. morphine, codeine, tramadol
Most effective pain relief but numerous side effects
Mechanism of action : Agonist of the endogenous opioid system
- Multiple sites of action -Brainstem (Disinhibition)
-Spinal cord
-Peripheral (inhibit channels on nociceptors)

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12
Q

What is gate control theory?

A

Modulation of pain at the spinal cord level

Pain evoked by nociceptors can be reduced by simultaneous activation of low threshold mechanoreceptors (Aβ fibres)
Simply rubbing/blowing on the painful area can reduce the pain sensation

Stimulation of Ab-fibres in vicinity of injury activates interneurons in dorsal horn, which inhibit spinothalamic neurons
C fibres inhibit inhibitory interneurons – opens gate
Aβ fibres activate inhibitory interneurons – closes gate

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13
Q

What is chronic pain?

A

Pain persists (>3 months)
Common - affects 20-50% OF THE POPULATION
E.g. Chronic back pain, cancer, carpal tunnel syndrome, arthritis, fibromyalgia, diabetes, migraine, post-surgery, multiple sclerosis, trigeminal neuralgia, phantom limb pain…

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14
Q

What types of chronic pain exists?

A

Inflammatory - persistent tissue inflammation

Neuropathic - Due to injury to nervous system

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15
Q

What are the symptoms of neuropathic pain?

A 
Burning 
Constant
Stabbing
Aching
Electricity/shocking
Spontaneous
Hypersensitivity
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16
Q

What are the main peripheral mechanisms of neuropathic pain?

A

Peripheral sensitization

Spontaneous firing of nociceptors

17
Q

Describe the spontaneous firing of nociceptors

A

Following a peripheral nerve injury, there is an increase in axonal firing at the injury site, due to:Accumulation of ion channels at regenerating tip of axon

  • Responsible for spontaneous pain
  • Underlies central neuropathic pain mechanisms
18
Q

List the main central mechanisms of neuropathic pain

A

Main central mechanisms:

  1. Central sensitization
    – within spinal cord
  2. Changes in activation patterns/cortical remapping
    – within brain
19
Q

Describe central sensitisation

A

Increase in the responsiveness of nociceptive neurons within the central nervous system
- Normal inputs begin to produce abnormal responses
Due to the reduced threshold for activation of 2nd order neurons (similar to LTP)

20
Q

Describe reduced threshold for activation of second order neurons

A

Constant firing of axons from the periphery
Sustained release of glutamate
Prolonged depolarisation of the postsynaptic membrane
Massive influx of Ca2+ through NMDA receptors
Activation of kinase
Phosphorylation of NMDA/AMPA receptors and channel protein synthesis
Alters kinetics of channels and causes insertion of more channels

21
Q

Describe the central hyperalgesia mechanism

A

Following central sensitization:

Activation of nociceptors results in amplified spinal cord activation

22
Q

Describe the central allodynia mechanism

A

Non-noxious Aβ fibres also synapse onto 2nd order spinothalamic neurons - Normally these are non-functional
Following central sensitization:
Non-noxious afferents activate sensitized 2nd order neurons

23
Q

What is the problem with central changes?

A

Not easily reversible

24
Q

Describe chronic pain treatments

A

Difficult to treat
Acute pain treatments often do not work
Good individual patient management is critical
Important to manage primary conditions and associated symptoms - Depression, sleep disturbance, fatigue

25
Q

List some current treatments for chronic pain

A 
Drugs:
		- Tricyclic antidepressants
		- Anticonvulsants
		- NMDA antagonists
			(All have analgesic properties)

Physiotherapy – e.g. manipulation of tissues, pacing

Psychological therapies – e.g. cognitive behavioral therapy

Surgery – e.g. spinal cord stimulator

26
Q

Describe tricyclic antidepressants and their mode of action

A

E.g. Amitriptyline

Mechanism of action:

- Unclear
- Act on descending inhibitory pathways
- Inhibits reuptake of serotonin (and noradrenalin)
27
Q

Describe anticonvulsants and their mechanism of action

A

Pregabalin / gabapentin, carbamazepine

Mechanism of action:

- Unclear
- Act in spinal cord to reduce excitability
- Blocks calcium (pregabalin/gabapentin) and sodium (carbomazepine) channels

Pregabalin/gabapentin do not act on GABAergic interneurons

- Blocks presynaptic voltage-gated Ca2+ channels
- Prevent release of glutamate from nociceptors
28
Q

What are NMDA antagonists and their mode of action?

A

Ketamine

Mechanism of action:

- NMDA receptor antagonist (reduces glutamate influx)
	- Prevents depolarization of second order neuron

- Adverse side effects (hallucinations/bad dreams)
29
Q

What are the NICE guidelines on the treatment of neuropathic pain

A

First-line of treatment:
- Amitriptyline or pregabalin

Second-line of treatment:
- Switch drugs or combine

Third-line of treatment:
- Refer patient to a specialist pain service and consider oral tramadol (opioid) or in combination with the second-line treatment consider topical lidocaine

30
Q

Describe the placebo effect of neuropathic pain

A

Placebo analgesia has been demonstrated (in well controlled studies) for the treatment of neuropathic pain
- Due to activation of descending inhibitory pathways

31
Q

List some complementary alternative therapies

A

Acupuncture, massage therapy, homeopathy, herbal medicine, hypnosis

Module 202 Theme 2 (12 decks)

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